Static exercise in untreated systemic hypertension.

Ewing, D J; Irving, John B.; Kerr, F; Kirby, B. J.

doi:10.1136/hrt.35.4.413

Cited by 73 publications

(27 citation statements)

References 8 publications

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“…On the basis of previous reports (Ewing, Irving, Kerr & Kirby, 1973;Hoel, Lorentzen & LundLarsen, 1970) the rise of both systolic and diastolic pressures, and of heart rate during static exercise was linear with time. Extrapolation of the values (accurately timed) to 60 s has been done, both for indirectly and directly obtained pressures.…”

Section: Methodsmentioning

confidence: 55%

Comparison of intra‐arterial and indirect blood pressures at rest and during isometric exercise in hypertensive patients before and after metoprolol.

Hunyor¹,

Nyberg²

1978

Brit J Clinical Pharma

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1. Blood pressure was measured both directly and indirectly in seven hypertensive patients before and after a single oral dose of 100 mg metoprolol, at rest and during sustained handgrip. 2. Intra‐arterially measured systolic and diastolic blood pressure increased linearly with time during sustained handgrip at 50% of maximal voluntary contraction. This linearity persisted for 60 s or more in most cases. Heart rate increased linearly for the first 30 s. 3. Indirectly measured blood pressure using an observer bias minimizing Auto‐Manometer, under‐read systolic and over‐read diastolic pressure both at rest and during handgrip. 4. By exact timing of recorded values during handgrip and linear extrapolation (or interpolation) from base‐line readings, mean values at 30 and 60 s of handgrip were calculated. The relationship between direct and indirect values remained the same at base‐line and 30 s of handgrip. At 60 s of handgrip, this was true only for diastolic pressure. For systolic pressure, indirect and direct values almost coincided. 5. After metoprolol, directly recorded pressure fell slightly (7–12 mm Hg, 0.02 less than P less than 0.10), both at rest and during handgrip, and heart rate fell by 15–18 beats/min (P less than 0.01). The systolic blood pressure and heart rate effect of metoprolol at 1 min handgrip correlated with peak plasma drug levels. Indirectly measured blood pressure did not change significantly. 6. The rate of rise in heart rate and blood pressure from base‐line to 60 s handgrip was not significantly influenced by metoprolol.

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Section: Methodsmentioning

confidence: 55%

Comparison of intra‐arterial and indirect blood pressures at rest and during isometric exercise in hypertensive patients before and after metoprolol.

Hunyor¹,

Nyberg²

1978

Brit J Clinical Pharma

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“…The mechanism of the dramatic increases in systolic and diastolic BPs observed with isometric muscular contraction is not clear (Donald et al, 1967;Lind, 1970;Ewing et al, 1973) but antihypertensive drugs do not seem to have a significant effect on this response (McDonald et al, 1966;Vecht et al, 1978;Taylor et al, 1979 (Richards et al, 1976) and therefore its effects may be reversed by increased sympathetic activity. This responses to controlled physiological stresses.…”

Section: Discussionmentioning

confidence: 99%

Effect of labetalol in hypertension during exercise and postural changes.

Balasubramanian¹,

Mann²,

Mw³

et al. 1979

Brit J Clinical Pharma

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1 Fourteen hypertensive patients were studied by intra-arterial BP monitoring to quantify the effects of standardized physiological stresses: Valsalva manoeuvre, isometric, treadmill and bicycle exercise, and 600 tilting before and after labetalol treatment. 2 The dose of labetalol ranged from 100-600 mg three times daily and the response was judged on outpatient clinic recordings. 3 The drug produced a sustained reduction of BP and heart rate responses during dynamic exercise and the Valsalva manoeuvre, but the degree of change from the lowered baseline were not changed by labetalol. The fall in BP on cessation of exercise was decreased rather than increased. 4 The response to controlled isometric muscle contraction was affected in a similar fashion. 5 Tilting produced a fall in BP after treatment, and this was most marked in those patients on the highest doses. However, compensatory increases in diastolic BP were observed.

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“…In some patients with hypertension or left ventricular dysfunction, as well as in certain elderly individuals, cardiac output does not rise, despite normal heart rate and pressor responses. In these patients, the pressure rise is accompanied by an increase in SVR (7)(8)(9)(10)(11) (12,13). Therefore, the present study was proposed in order to (a) delineate the effector mechanism of heart rate control during SHG; (b) explore the mechanism of the pressor response and the possible role of sympathetically mediated vasoconstriction; and (c) evaluate left ventricular performance by the technique of systolic time intervals during SHG, before and after autonomic blockade.…”

Section: Introductionmentioning

confidence: 99%

Autonomic Mechanisms in Hemodynamic Responses to Isometric Exercise

Martin¹,

Shaver²,

Leon³

et al. 1974

J. Clin. Invest.

202

113

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A B S T R A C T Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve.The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemoPortions of this study were presented previously in abstract form.

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Static exercise in untreated systemic hypertension.

Cited by 73 publications

References 8 publications

Comparison of intra‐arterial and indirect blood pressures at rest and during isometric exercise in hypertensive patients before and after metoprolol.

Comparison of intra‐arterial and indirect blood pressures at rest and during isometric exercise in hypertensive patients before and after metoprolol.

Effect of labetalol in hypertension during exercise and postural changes.

Autonomic Mechanisms in Hemodynamic Responses to Isometric Exercise

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